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3rd Year Dermatology PG Theory Examination

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Q1. Discuss the Characteristics of 'Polar' Leprosy Lesions [10 Marks]

Introduction (1 mark)

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Basis of Polarity (1 mark)

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A. Polar Tuberculoid Leprosy (TT) [3 marks]

• Fewer than 5 lesions (usually 1-3), often just a single lesion
• Well-defined, sharply demarcated borders with a raised, erythematous edge
• Hypopigmented or erythematous in color
• Surface is dry, rough, and scaly due to autonomic nerve involvement
• Lesions are anesthetic (complete loss of all modalities) and anhidrotic
• Satellite lesions are absent

• Peripheral nerve thickening is marked and asymmetric
• Commonly affected nerves: greater auricular nerve, superficial peroneal nerve, ulnar nerve
• Early neurological deficit: wasting of interossei, thenar and hypothenar eminences
• Claw hand (ulnar), footdrop (lateral popliteal), lagophthalmos (facial nerve)
• "Pure neuritic leprosy" may occur with no skin lesions

• Well-formed epithelioid granulomas with Langhans giant cells
• Dense lymphocytic mantle surrounding granulomas
• Nerves within dermis are destroyed and replaced by epithelioid cells
• AFB: absent or extremely rare (paucibacillary)

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B. Polar Lepromatous Leprosy (LL) [3 marks]

• Numerous (too many to count), symmetrically distributed lesions
• Poorly defined, ill-defined borders - macular, papular, nodular, plaque-type
• Early: erythematous macules bilaterally symmetric, especially on face, buttocks, and extremities
• Late: nodules and plaques coalesce - leonine facies (facial infiltration giving lion-like appearance)
• Ear lobe infiltration is characteristic
• Madarosis: loss of lateral eyebrows (earliest sign) and eyelashes

• Saddle nose deformity due to nasal mucosal infiltration and septal collapse
• Acquired ichthyosis on lower extremities
• Anesthesia in glove and stocking distribution (late, symmetric)
• Eye: lagophthalmos, keratitis, corneal anesthesia, iris pearls
• Testicular infiltration: gynecomastia, infertility
• Laryngeal involvement: hoarseness

• LLp (polar LL): stable; does not upgrade
• LLs (subpolar LL): retains some CMI; may show reactional episodes

• Diffuse sheets of foamy macrophages (Virchow cells/lepra cells) filled with bacilli
• No granuloma formation; lymphocytes sparse and displaced to periphery
• AFB: strongly positive; Globi (clusters of bacilli within macrophages) seen on Fite-Faraco stain
• Grenz zone: uninvolved clear zone of upper dermis separating epidermis from infiltrate

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Summary Table (1 mark)

• Andrews' Diseases of the Skin, pp. 396-398; Dermatology 2-Volume Set 5e, pp. [block17]

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Q2. Discuss 'Reactions in Leprosy' [10 Marks]

Introduction (1 mark)

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Classification [1 mark]

1. Type 1 Reaction - Reversal Reaction (RR)
2. Type 2 Reaction - Erythema Nodosum Leprosum (ENL)
3. Lucio Phenomenon - A third type seen in diffuse lepromatous leprosy

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A. Type 1 Reaction - Reversal Reaction [3 marks]

• Represents a delayed-type hypersensitivity (DTH) reaction with a Th1 cytokine pattern
• Sudden upsurge in CMI against M. leprae antigens
• Associated with "upgrading" reactions (shift toward tuberculoid pole) or "downgrading" (deterioration toward lepromatous)

• Occurs in borderline leprosy patients (BT, BB, BL) - the most common reactive group
• Also seen in recovering tuberculoid patients with immunologic recovery

• Preexisting skin lesions become acutely inflamed, swollen, erythematous, and edematous
• Lesions may ulcerate in severe cases
• Acute neuritis is the most feared complication: acute nerve pain, nerve tenderness, and sudden loss of sensory and motor function
• "Hot" abscess of nerve trunk may form (distinct from "cold" abscess of TT leprosy)
• No new lesions appear - only established lesions become inflamed
• Systemic symptoms are minimal

• Prednisolone 40 mg/day, tapered over 12-36 weeks (protocol varies by MB vs. PB and severity)
• MDT must be continued without interruption
• Ophthalmological care for lagophthalmos

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B. Type 2 Reaction - Erythema Nodosum Leprosum (ENL) [3 marks]

• Represents excessive humoral immunity with a Th2 cytokine pattern and immune complex deposition (Type III hypersensitivity)
• High circulating antigen from bacillary death triggers complement activation
• Neutrophil infiltration into ENL lesions is characteristic
• Can also be accompanied by increased CMI

• Occurs in lepromatous (LL) and borderline lepromatous (BL) leprosy
• More common in patients with high bacterial index
• Can be precipitated by MDT, intercurrent infection, stress, surgery, or pregnancy

• New crops of tender, erythematous papules and subcutaneous nodules
• Appear on any part of the body (not restricted to preexisting lesions - key distinction from Type 1)
• Can become pustular, bullous, or ulcerative in severe cases

• Fever, malaise, myalgia (often high-grade)
• Iridocyclitis (can lead to blindness)
• Orchitis (acute scrotal pain and swelling)
• Lymphadenitis, hepatosplenomegaly
• Arthritis - severe joint swelling and pain
• Glomerulonephritis - may lead to proteinuria and renal impairment
• Dactylitis, peripheral edema, laryngeal involvement
• Secondary amyloidosis is a long-term complication of recurrent ENL

• Mild ENL: NSAIDs + rest
• Severe ENL: Thalidomide 400 mg/day orally, tapered once controlled (avoid in women of childbearing age due to teratogenicity)
• Prednisolone 40-60 mg/day if thalidomide unavailable or contraindicated
• Clofazimine has anti-inflammatory properties and helps prevent recurrences (dose: up to 300 mg/day for several months)
• MDT must continue throughout

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C. Lucio Phenomenon [1 mark]

• Occurs exclusively in patients with diffuse non-nodular lepromatous leprosy (Lucio leprosy), particularly from Mexico and Central America
• Pathogenesis: ischemic necrosis due to vascular endothelial infiltration by M. leprae with secondary endarteritis and thrombosis
• Clinically: retiform (star-shaped) purpura progressing to painful necrotic ulcers
• Systemic vasculitis may develop
• Treatment: supportive; wound care; MDT; systemic steroids in severe cases; plasmapheresis reported

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Comparison Table [1 mark]

• Dermatology 2-Volume Set 5e, Table 75.3; Goodman & Gilman's, p. [block17]

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Q3. Elaborate the Management of a Case of Multibacillary Leprosy [10 Marks]

Introduction (1 mark)

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Goals of Treatment [1 mark]

1. Kill M. leprae and render the patient non-infectious
2. Prevent drug resistance (rationale for combination therapy)
3. Prevent and manage disability and reactions
4. Achieve social rehabilitation

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WHO MDT Regimen for Multibacillary Leprosy [3 marks]

• Duration: 12 months (MB blister packs, to be completed within 18 months)

• Rifampicin 450 mg monthly (supervised)
• Dapsone 50 mg daily (self-administered)
• Clofazimine 150 mg monthly (supervised) + 50 mg alternate days

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Mechanism of Action of MDT Drugs [2 marks]

• Inhibits bacterial DNA-dependent RNA polymerase
• Kills ~99.9% of viable bacilli within days of the first dose; renders patient non-infectious rapidly
• Essential for preventing drug resistance

• A sulfone that inhibits dihydropteroate synthase (competitive inhibitor of PABA utilization), blocking folate synthesis
• Active against both solid (viable) and fragmented (dead) bacilli

• Binds preferentially to mycobacterial DNA
• Generates reactive oxygen species
• Has important anti-inflammatory properties that help prevent and dampen lepra reactions (Type 2/ENL)
• Notable side effect: reversible reddish-brown to slate-grey skin discoloration and ichthyosis

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Management of Special Situations [1 mark]

• Pregnancy: MDT is safe and should be continued. Leprosy may worsen during and post-partum.
• HIV co-infection: MDT is not contraindicated; management and response to MDT are the same as in HIV-negative patients.
• Defaulters: If patient returns with one or more active signs (raised/reddened lesions, new lesions, new nerve involvement, nodules, reaction signs), restart a full new 12-month course.
• Relapse: Defined as development of new active lesions after a documented cure. Treat with full MDT again.

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Management of Reactions During Treatment [1 mark]

• Continue MDT without interruption during any reaction
• Type 1 reaction: Prednisolone 40 mg/day, tapered over 12-36 weeks
• Type 2 (ENL): Thalidomide (severe) or prednisolone; clofazimine dose may be increased to 300 mg/day

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Prevention of Disability [1 mark]

• Regular nerve function assessment (sensory + motor testing)
• Eye protection in lagophthalmos (lubricating drops, protective glasses, lateral tarsorrhaphy if needed)
• Physiotherapy and occupational therapy for deformities
• Protective footwear for insensitive feet
• Reconstructive surgery for fixed deformities (e.g., tendon transfers, claw hand correction)

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Monitoring and Follow-up

• Slit-skin smear (SSS) at baseline and annually; Bacterial Index (BI) should decline 1+ per year
• If BI does not fall or rises, suspect resistance or re-infection
• Drug resistance testing (rifampicin resistance via PCR) for non-responders
• Park's Textbook of Preventive & Social Medicine, pp. 2367-2432; Goldman-Cecil Medicine, Table 301-3; Andrews' Diseases of the Skin, p. 4556

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Q4. Discuss Antiretroviral Treatment [10 Marks]

Introduction (1 mark)

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Principles of ART [1 mark]

1. ART should be initiated as soon as possible after HIV diagnosis (regardless of CD4 count)
2. Exception: delay by 2-4 weeks in active TB, and by 4-6 weeks in cryptococcal meningitis
3. Three-drug combinations are standard (prevents resistance)
4. Goal: achieve undetectable viral load (<50 copies/mL)
5. Adherence is paramount - poor adherence leads to resistance

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Classes of Antiretroviral Drugs [5 marks]

1. Nucleoside/Nucleotide Reverse Transcriptase Inhibitors (NRTIs/NtRTIs)

• Tenofovir disoproxil fumarate (TDF) - NtRTI; nephrotoxic; avoid in renal impairment
• Tenofovir alafenamide (TAF) - better renal and bone profile than TDF
• Abacavir (ABC) - HLA-B*5701 testing required; risk of hypersensitivity reaction
• Lamivudine (3TC) and Emtricitabine (FTC) - well tolerated; also active against Hepatitis B
• Zidovudine (ZDV/AZT) - first antiretroviral; causes bone marrow suppression, anemia, myopathy

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2. Non-Nucleoside Reverse Transcriptase Inhibitors (NNRTIs)

• Efavirenz (EFV) - once daily; CNS side effects (vivid dreams, dizziness), teratogenic (avoid 1st trimester)
• Nevirapine (NVP) - significant hepatotoxicity (especially in women with CD4 >250); skin rashes/SJS
• Rilpivirine (RPV) - better tolerated; requires adequate stomach acid (take with food); do not use if VL >100,000
• Etravirine (ETR) - active against some NNRTI-resistant strains
• Doravirine (DOR) - newer; fewer CNS effects

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3. Protease Inhibitors (PIs)

• Darunavir (DRV) - most widely used; always boosted with ritonavir or cobicistat
• Atazanavir (ATV) - causes benign hyperbilirubinemia (jaundice)
• Lopinavir/ritonavir (LPV/r) - used in pregnancy; GI side effects

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4. Integrase Strand Transfer Inhibitors (INSTIs)

• Dolutegravir (DTG) - first-line recommended; high barrier to resistance; once daily; neural tube defect risk if used periconceptionally
• Bictegravir (BIC) - newer; available as Biktarvy (BIC/TAF/FTC)
• Raltegravir (RAL) - first INSTI approved; twice daily
• Elvitegravir (EVG) - requires pharmacokinetic boosting

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5. Entry Inhibitors [1 mark]

• Enfuvirtide (T-20): Binds gp41 on HIV envelope; prevents fusion of viral envelope with CD4+ T cell membrane; injectable; used in salvage therapy

• Maraviroc (MVC): Blocks CCR5 co-receptor on CD4+ cells; requires tropism testing first (only if virus is R5-tropic, not X4-tropic)

• Ibalizumab: Monoclonal antibody against CD4 receptor (post-attachment); used in drug-resistant HIV

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Recommended First-Line Regimen [1 mark]

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When to Switch Regimens [1 mark]

• Virologic failure: Viral load >50 copies/mL on two consecutive tests despite adherence
• Toxicity/intolerance: Switch to a drug in the same or different class
• Drug resistance: Prior to switching, genotypic resistance testing guides new regimen selection
• Always include at least 2 fully active drugs in a new regimen
• Harrison's Principles of Internal Medicine 22E, pp. 2044-2049; Goldman-Cecil Medicine, Table 357-1

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Q5. Discuss the Pathogenesis of Early Syphilis [10 Marks]

Introduction (1 mark)

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The Organism [1 mark]

• An obligate human pathogen (cannot be cultured on artificial media)
• A thin, tightly coiled spirochete 6-20 μm long, 0.1-0.2 μm wide
• Highly motile via endoflagella
• Outer membrane has few surface-exposed proteins (aiding immune evasion)
• Divides slowly (every 30-33 hours), explaining the indolent course

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Step 1: Inoculation and Epithelial Breach [1 mark]

• Transmission occurs through direct contact with infectious cutaneous or mucosal lesions (chancre or condylomata lata) during sexual activity
• T. pallidum enters through microscopic abrasions in skin or intact mucous membranes
• Minimal inoculum (~57 organisms) is required for infection
• The incubation period is 9-90 days (mean 21 days) before the primary chancre appears

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Step 2: Local Adhesion and Invasion [1 mark]

• After entry, spirochetes bind to host cells via fibronectin-binding proteins (e.g., TROMP1/Tp0155) on their outer membrane
• They also bind to laminin and collagen within the extracellular matrix
• T. pallidum rapidly penetrates sub-epithelial tissue by boring through intercellular junctions using corkscrew motility
• Hyaluronidase production helps further tissue invasion

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Step 3: Rapid Systemic Dissemination (before chancre appears) [1 mark]

• This is a critical concept: spirochetes disseminate via lymphatics and the bloodstream even before the primary lesion appears
• T. pallidum survives in the bloodstream due to its paucity of surface proteins (few antigens exposed = poor immunogenicity)
• Organisms seed to distant organs: skin, liver, bone, eyes, CNS, placenta
• This explains why anti-syphilitic therapy started late can still fail to prevent tertiary complications

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Step 4: Primary Syphilis - Chancre Formation [2 marks]

• 21 days (range 9-90 days) after inoculation, the chancre appears at the site of spirochetal entry
• Spirochetes are plentiful within the chancre

• The pathognomonic lesion of syphilis at all stages is obliterative endarteritis with a plasma-cell-rich inflammatory infiltrate
• Endothelial cell activation and proliferation (driven by host immune response, not direct spirochetal toxicity) cause progressive luminal narrowing
• This leads to ischemic necrosis of overlying tissue and erosion to form the ulcer
• The surrounding induration results from edema and the dense inflammatory infiltrate (predominantly lymphocytes and plasma cells)

• Slightly elevated, firm, painless papule that erodes to form a clean-based, shallow ulcer
• Surrounding cartilaginous induration (buttonlike mass) = "hard chancre"
• 70% of men: on penis or scrotum
• 50% of women: on vulva or cervix (often asymptomatic if on cervix)
• Oral, anal, and rectal chancres also occur
• Painless regional lymphadenopathy (bilateral, rubbery, non-tender) accompanies the chancre

• The host mounts a humoral (seroconversion ~3-6 weeks) and cellular immune response
• However, this immune response fails to eradicate T. pallidum
• Chancre resolves spontaneously in 2-6 weeks even without treatment
• Resolution reflects local immune containment, not cure - spirochetes persist in distant sites

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Step 5: Secondary Syphilis - Systemic Immune-Mediated Damage [2 marks]

• Develops approximately 4-10 weeks after the chancre (sometimes while chancre is still present)
• About 25% of untreated primary syphilis patients develop secondary syphilis
• The abundant spirochetemia at this stage drives immune complex deposition and widespread tissue injury

• Generalized rash: discrete red-brown macules (<5 mm) - characteristically involves palms and soles (pathognomonic)
• Papulosquamous, annular, or pustular variants
• Condylomata lata: Broad, elevated, flat-topped, moist, highly infectious plaques in moist flexural areas (perianal, perineal, axillae) - rich in spirochetes
• Mucous patches: Grayish-white erosions on oral/genital mucosa
• "Split papules": at angles of mouth

• Characteristic proliferative endarteritis with lymphocytes and plasma cells
• Spirochetes abundant in skin and mucous membrane lesions on Warthin-Starry/Steiner stain or immunohistochemistry

• Generalized lymphadenopathy (neck and inguinal most common)
• Germinal center hyperplasia + plasma cell infiltration of nodes
• Constitutional symptoms: fever, malaise, headache, sore throat ("great imitator")
• Hepatitis (elevated transaminases)
• Nephropathy (membranous glomerulonephritis via immune complexes)
• Iritis/uveitis (ocular syphilis)
• Aseptic meningitis (early neurosyphilis)
• Arthritis, periostitis

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Role of the Immune Evasion Mechanisms [1 mark]

• Paucity of surface-exposed proteins - outer membrane has very few lipoproteins (unlike most bacteria); minimal TLR stimulation
• Molecular mimicry - surface phospholipids resemble host membranes
• Intracellular location - persists within endothelial cells and fibroblasts
• Produces no endotoxin or exotoxin; tissue damage is immune-mediated
• Can cross the blood-brain barrier early, establishing a reservoir in the CNS

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Summary [1 mark]

Inoculation via mucosa/skin breach
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Local adhesion via fibronectin-binding proteins
        ↓
Rapid hematogenous + lymphatic spread (even before chancre)
        ↓ (~21 days)
Chancre: endarteritis → ischemic necrosis → painless ulcer
        ↓ (4-10 weeks, if untreated)
Secondary syphilis: disseminated immune complex disease
palmar-plantar rash, condylomata lata, systemic features
        ↓
Early latent syphilis (seropositivity without symptoms)

• Non-treponemal (VDRL/RPR): Positive by ~3 weeks after chancre; titer correlates with disease activity
• Treponemal (FTA-ABS, TPPA): Positive early; remain positive for life
• Robbins & Kumar Basic Pathology, pp. 669-671 (Syphilis)

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Q6. Discuss Clinical Features and Treatment Modalities of Anogenital Warts [10 Marks]

Introduction (1 mark)

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Virology and Epidemiology (1 mark)

• HPV is a non-enveloped, double-stranded DNA virus of the Papillomaviridae family
• Over 200 HPV subtypes exist; ~40 infect the anogenital tract
• Approximately 14 million new infections occur annually in the USA alone
• Up to 80% of sexually active adults will acquire genital HPV infection in their lifetime
• Most infections clear spontaneously within 1-2 years; persistence leads to warts or malignancy
• Peak incidence in ages 17-33 years

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Clinical Features [4 marks]

A. Sites of Involvement

• External genitalia: labia minora, labia majora, clitoris, vaginal introitus
• Perineum and perianal skin
• Vagina (10-30% of cases)
• Cervix (7% of cases) - flat condylomata
• Urethra (meatus)

• Penile shaft (most common), glans, coronal sulcus, frenulum
• Prepuce/foreskin
• Urethral meatus (5-10%)
• Perianal and anal canal (especially in men who have sex with men)
• Scrotum

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B. Morphological Types

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C. Symptoms

• Many patients are asymptomatic - lesions discovered incidentally
• Pruritus - the most common symptom (especially perianal warts)
• Bleeding after intercourse or defecation (anal/cervical warts)
• Discharge from vaginal or urethral lesions
• Dyspareunia (vaginal warts)
• Difficulty urinating/dribbling (urethral meatal warts)
• Hoarseness/stridor (laryngeal papillomatosis - recurrent respiratory papillomatosis in children born to infected mothers)
• Psychological distress, stigma, and anxiety

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D. Special Clinical Situations

• Pregnancy: Warts may enlarge dramatically due to immunosuppression and increased vascularity. Can obstruct the birth canal. Cesarean section if warts obstruct. Risk of juvenile recurrent respiratory papillomatosis in neonates if delivered vaginally.
• HIV/immunocompromised: Warts are larger, more numerous, more refractory to treatment, and have higher rate of malignant transformation
• Children with anogenital warts: Must consider sexual abuse; though vertical transmission and fomite transmission are also possible
• Bowenoid papulosis: Multiple small, flat-topped, brownish-red papules; associated with HPV-16; histology shows full-thickness dysplasia (carcinoma in situ); mainly in young sexually active adults; treated by destructive methods

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E. Diagnosis

• Usually clinical (visual inspection); biopsy not routinely needed
• Acetowhitening (3-5% acetic acid application): turns HPV-infected epithelium white - useful for subclinical lesions
• Colposcopy for cervical and vaginal lesions
• Biopsy indicated for: pigmented lesions, treatment failure, atypical morphology, immunocompromised patients, suspicion of malignancy
• Histology: Hyperkeratosis, acanthosis, papillomatosis, and characteristic koilocytes (large squamous cells with perinuclear clearing/halo and wrinkled "raisinoid" nuclei)
• HPV DNA testing (PCR) for high-risk types in cervical screening programs

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Treatment Modalities [4 marks]

A. Patient-Applied Therapies

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B. Provider-Applied Therapies

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C. Systemic and Emerging Therapies

• Cidofovir (intralesional or topical): for refractory/HIV-associated warts
• Photodynamic therapy (PDT): 5-ALA + visible light; effective for flat/mucosal lesions
• Bleomycin intralesional: cytotoxic; for resistant warts

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D. Prevention - HPV Vaccination (1 mark)

• Gardasil-9 (9-valent: HPV 6, 11, 16, 18, 31, 33, 45, 52, 58): Recommended for males and females aged 9-26 years; best given before sexual debut; 2-dose schedule if <15 years; 3-dose if ≥15 years or immunocompromised
• Gardasil-4 (Quadrivalent): Covers HPV 6, 11, 16, 18 - prevents >90% of anogenital warts
• Cervarix (Bivalent, HPV 16, 18): Only for cervical cancer prevention; does not prevent warts
• Condom use reduces (but does not eliminate) transmission
• Bailey & Love's Surgery, p. 9782; Andrews' Diseases of the Skin, Chapter 19

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Q7a. Eye Involvement in Leprosy [5 Marks]

Introduction (0.5 mark)

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Mechanisms of Eye Involvement (1 mark)

1. Direct invasion by M. leprae - primarily in lepromatous leprosy
2. Nerve damage - involvement of facial nerve (CN VII) and trigeminal nerve (CN V) branches
3. Lepra reactions - especially Type 2 (ENL) causing acute iridocyclitis

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Clinical Features [3 marks]

A. Eyelids

• Madarosis: Loss of eyebrows and eyelashes - earliest and most characteristic sign; due to lepromatous infiltration of hair follicles (lateral > medial eyebrow)
• Ptosis: Ectropion or entropion due to orbicularis oculi weakness (facial nerve involvement)
• Infiltration of skin of eyelids in LL

B. Facial Nerve (CN VII) - Branch to Orbicularis Oculi

• Lagophthalmos: Inability to fully close the eyelids due to paralysis of orbicularis oculi (lower division of facial nerve)
• Most important cause of blindness in leprosy
• Exposes the cornea to desiccation, trauma, and infection
• Leads to exposure keratopathy: punctate keratitis → corneal ulceration → perforation → blindness
• "Sleeping open-eyed" or nocturnal lagophthalmos is particularly dangerous

C. Trigeminal Nerve (CN V) - Ophthalmic Branch

• Corneal anesthesia: Loss of corneal sensation; patient cannot feel foreign bodies → repeated micro-trauma without protective reflexes
• Leads to neuroparalytic keratitis (neurotrophic keratopathy)
• Combined lagophthalmos + corneal anesthesia = very high risk of blindness (dangerous combination)

D. Iris, Ciliary Body, and Anterior Segment

• Acute iridocyclitis (anterior uveitis): Most commonly during ENL (Type 2 reaction); presents with pain, photophobia, circumcorneal congestion, hypopyon
• Chronic iridocyclitis (insidious): Gradual, painless; leads to posterior synechiae, iris atrophy
• "Iris pearls" (lepromata of iris): Pathognomonic white/yellow nodular deposits of M. leprae-laden macrophages on anterior iris surface; virtually diagnostic of lepromatous leprosy
• Pupillary miosis: Due to direct leprous infiltration of the ciliary muscle/iris sphincter; small, fixed, irregular pupil
• Hypopyon, hyphema (in severe reactions)

E. Other Ocular Structures

• Scleritis and episcleritis: In ENL reactions
• Corneal lepromata: Superficial, small, whitish opacities in the cornea (avascular stroma) due to direct bacillary infiltration in LL
• Glaucoma: Secondary to chronic iridocyclitis and posterior synechiae
• Cataract: Secondary to chronic uveitis or steroid use
• Lacrimal gland involvement: Dry eye (keratoconjunctivitis sicca) from dacryoadenitis

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Prevention and Management (0.5 mark)

• Regular ophthalmological assessment at every clinic visit
• Corneal sensation testing (cotton wisp), Bell's reflex, and visual acuity measurement
• Lagophthalmos: Protective glasses, lubricating eye drops (artificial tears), lid-taping at night; lateral tarsorrhaphy (surgical) for severe cases
• Acute iridocyclitis (ENL): Topical/systemic corticosteroids + cycloplegics (atropine 1% eye drops)
• Corneal ulceration: Topical antibiotics, patching, urgent ophthalmology referral
• Reconstructive lid surgery (tarsal strip, brow lift) for severe lagophthalmos with good visual prognosis

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Q7b. Histology of Borderline Leprosy [5 Marks]

Introduction (0.5 mark)

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General Principles (0.5 mark)

• Skin biopsy is taken from an active edge of a lesion, fixed in formalin, and stained with H&E and Fite-Faraco (modified Ziehl-Neelsen for M. leprae)
• Histological features in borderline leprosy share elements of both granulomatous (tuberculoid) and histiocytic (lepromatous) patterns
• The Bacterial Index (BI) on Fite-Faraco increases from BT to BL: BT (0-1+), BB (1-2+), BL (2-4+)

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A. Borderline Tuberculoid (BT) [1 mark]

• Well-formed epithelioid cell granulomas (similar to TT, but less well-organized)
• Langhans giant cells are present but fewer than in TT
• Dense lymphocytic infiltrate surrounds the granulomas
• Nerves show epithelioid infiltration but are not completely replaced - "onion-skin" perineural infiltration begins to appear
• Nerves within dermis are recognizable (unlike TT where they are totally destroyed)
• Grenz zone (subepidermal clear zone) is absent (like TT)
• AFB: negative or very rare (0-1+)

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B. Mid-Borderline (BB) [1 mark]

• Poorly formed epithelioid granulomas - the most characteristic feature
• No giant cells (absent or extremely rare) - key distinguishing feature from BT
• Lymphocytes are scattered and not tightly packed; lymphocyte number decreasing
• Macrophages show intermediate morphology - between epithelioid and foamy types
• Nerve involvement: Perineural "onion-skin" laminated proliferation is prominent; nerve infiltrated but recognizable
• Grenz zone begins to appear (incomplete, narrow)
• AFB: 1-2+ (moderate); bacilli are present but not forming globi
• Highly unstable histologically - difficult to definitively classify

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C. Borderline Lepromatous (BL) [1.5 marks]

• Sheets of epithelioid macrophages mixed with lymphocytes
• Granulomas are ill-formed or absent in some areas
• Foamy macrophages (early Virchow cell formation) begin to appear - incomplete, not as lipid-laden as in LL
• Lymphocytes still present (unlike LL where they are sparse), but displaced to the periphery
• Grenz zone is well-established - a clear, uninvolved subepidermal zone separates the dermis from the epidermis
• Perineural laminated fibrosis ("onion-skin") is prominent - nerves show concentric layering of fibroblasts and collagen around nerve bundles; nerves still identifiable
• AFB: 2-4+ (many); bacilli visible within macrophages, beginning to form small clusters (early globi)
• Eroded epidermis above lesions may show flattened rete ridges

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D. Reactional Changes in Borderline Histology (1 mark)

• Pre-existing granulomas become edematous with increased lymphocytic infiltration
• Nerve bundles show acute inflammatory infiltrate - edema, polymorphonuclear cells
• Granulomas upgrade: BB lesions acquire more Langhans giant cells (moving toward BT pattern)
• Vascular congestion and dermal edema

• Granulomas become less organized
• Lymphocytes decrease; foamy macrophages increase
• AFB increases

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Summary Table (0.5 mark)

• Andrews' Diseases of the Skin, pp. 4289-4313; Fitzpatrick's Dermatology, block25

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Q8a. Indeterminate (Intermediate) Leprosy [5 Marks]

Introduction (0.5 mark)

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Epidemiology and Significance (0.5 mark)

• The earliest skin lesion that appears after exposure to M. leprae
• All patients with subsequent clinical leprosy pass through an indeterminate phase before the immune response "sets"
• Spontaneous resolution occurs in 75% of cases without treatment
• The remaining 25% progress to determinate leprosy (TT, BT, BB, BL, or LL), determined by the individual's CMI
• Children are particularly prone to develop this stage after household contact exposure

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Clinical Features [2 marks]

• A single (or occasionally few), poorly defined, hypopigmented macule - the most common presentation
• The macule merges gradually with surrounding normal skin - ill-defined borders (unlike TT where borders are sharply defined)
• Surface is smooth - no surface roughness or scaling
• Color is faint, lighter than surrounding skin; may appear erythematous in fair-skinned individuals
• Size: Usually 2-10 cm in diameter
• Common sites: Cheeks, buttocks, upper arms, outer thighs, trunk

• Sensation may be normal or minimally altered (unlike TT where there is complete anesthesia)
• Subtle decrease in temperature discrimination may be detected
• Sweating may be mildly reduced (hypohidrosis) within the lesion
• Anhidrosis is incomplete and inconsistent

• Peripheral nerves are not enlarged at this stage
• No plaques, nodules, or papules
• No muscle weakness or atrophy

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Investigations [1 mark]

• Slit-skin smear (Fite-Faraco stain): AFB negative (bacillary load too low)
• Lepromin test (Mitsuda test): Variable - may be positive, negative, or weakly positive; not diagnostic but prognostic (positive result predicts progression to tuberculoid; negative predicts lepromatous)
• Histology (skin biopsy): Small, non-specific lymphocytic infiltrate around skin appendages (hair follicles, sweat glands), around blood vessels and nerves; no granuloma formation - this is the defining histological feature; lymphocytes scattered in dermis; perineural lymphocytic infiltration in small nerves; AFB negative; changes are non-diagnostic in isolation
• PCR for M. leprae DNA: Positive in some cases; useful research tool but not routinely available
• Nerve conduction studies: Usually normal

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Differential Diagnosis (0.5 mark)

• Pityriasis versicolor (KOH positive; scale present)
• Pityriasis alba (childhood; common on face; no sensation loss)
• Post-inflammatory hypopigmentation
• Vitiligo (complete depigmentation; milk-white; Wood's lamp fluorescence)
• Tinea corporis (scale; KOH positive)
• Nevus depigmentosus (present from birth)

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Treatment and Prognosis (0.5 mark)

• WHO MDT for paucibacillary leprosy: Rifampicin 600 mg once monthly + Dapsone 100 mg daily for 6 months
• Early treatment halts progression and prevents disability
• Most lesions resolve completely with treatment, leaving possible residual pigmentary changes
• Without treatment, majority (75%) resolve spontaneously; minority progress

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Q8b. Mycobacterium leprae [5 Marks]

Introduction (0.5 mark)

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Morphology and Staining [1 mark]

• Gram-positive bacterium (poorly Gram-staining due to waxy cell wall)
• Shape: Straight or slightly curved rod; 3-7 μm long, 0.3-0.5 μm wide - smaller than other mycobacteria
• Strongly acid-fast - retains carbol fuchsin dye despite acid-alcohol decolorization
• Special stain: Fite-Faraco stain (modified Ziehl-Neelsen - milder decolorizer) - stains red on blue background; regular ZN is too harsh and decolorizes M. leprae
• Beaded or granular appearance within macrophages (viable bacilli stain solidly; dead/fragmented bacilli appear granular or beaded)
• Found in tissues predominantly within macrophages and Schwann cells of peripheral nerves
• In lepromatous leprosy: forms globi - large clusters of bacilli packaged in "cigar bundle" arrangement within macrophage vacuoles
• Morphological Index (MI): Percentage of solid-staining (viable) bacilli out of total; normal MI declines with effective treatment; MI >1% suggests treatment failure or relapse

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Cultural and Biological Properties [1 mark]

• Cannot be cultured on artificial media - obligate intracellular parasite; all metabolic enzymes required for replication depend on host cell environment
• In vitro cultivation remains impossible despite decades of effort - a major limitation in research
• Experimental animal models:
  • Armadillo (Dasypus novemcinctus): Nine-banded armadillo; naturally susceptible; develops disseminated LL-like disease; used for large-scale production of M. leprae for research; core body temperature ~30-32°C matches M. leprae optimum
  • Mouse foot-pad model (Shepard model, 1960): Inoculation into mouse footpad produces limited local multiplication; used for drug sensitivity testing and viability studies
  • Nude (athymic) mice: Allow more extensive multiplication

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Genome and Metabolism [1 mark]

• Genome size: 3.27 Mb - one of the smallest genomes among mycobacteria
• Massive reductive evolution: ~50% of genome is non-functional (pseudogenes); has lost many genes for biosynthetic and metabolic pathways
• Doubling time: 11-14 days - the slowest of all known pathogens; explains the long incubation period (3-5 years average) and chronic indolent disease
• Optimal growth temperature: 27-30°C - explains predilection for skin, peripheral nerves, anterior chamber of eye, and upper respiratory tract (cooler body areas)
• Does not survive outside the human body for long; nasal secretions can contain live bacilli
• Phenolic glycolipid-1 (PGL-1): Unique surface antigen; present only on M. leprae; helps bacillus bind to laminin in Schwann cell basal lamina; used in serodiagnosis (anti-PGL-1 IgM antibodies in lepromatous leprosy); contributes to immunosuppression

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Pathogenicity and Immune Evasion [1 mark]

• Tropism for Schwann cells: M. leprae binds to the G domain of laminin-α2 on Schwann cell basal lamina via PGL-1 and histone-like proteins; enters Schwann cells where it survives intracellularly; demyelination and axonal degeneration follow
• Immunosuppression: PGL-1 scavenges reactive oxygen intermediates (ROI); lipoarabinomannan (LAM) suppresses macrophage activation by inhibiting IFN-γ-induced signaling; inhibits antigen presentation
• Survives within macrophages by preventing phagosome-lysosome fusion
• Nerve predilection explains the unique feature of leprosy among bacterial infections - peripheral neuropathy is the hallmark

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Transmission and Epidemiology (0.5 mark)

• Route of transmission: Primarily via respiratory droplets from nasal secretions of untreated lepromatous patients (bacilli in nasal discharge up to 10⁷/mL)
• Skin-to-skin contact via broken skin is a secondary route
• Entry is through nasal mucosa or broken skin
• Incubation period: 2-12 years (average 5 years) - due to the extremely slow replication rate
• Contact infection risk: 5-10% in household contacts of MB leprosy; <1% in general population
• Source: Zoonotic reservoir exists in wild armadillos and non-human primates
• Harrison's Principles of Internal Medicine 22E; Andrews' Diseases of the Skin

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Q9a. Genital Herpes Complicating Pregnancy [5 Marks]

Introduction (0.5 mark)

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Epidemiology and Timing (0.5 mark)

• HSV-2 causes 70-85% of genital herpes; HSV-1 is increasingly responsible
• Primary genital herpes during pregnancy: risk of neonatal transmission 26-56% (highest risk)
• Recurrent genital herpes with active lesions at delivery: neonatal transmission risk 2-5%
• 70% of mothers of infants with neonatal herpes are asymptomatic at delivery
• Incidence of neonatal herpes: 1 in 3,200 live births

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Maternal Risks During Pregnancy [1 mark]

• First trimester: Risk of spontaneous abortion (~20%), embryonic fetal death
• Second/third trimester: Premature labor, premature rupture of membranes (PROM), fetal growth restriction
• Disseminated maternal HSV: Rare but life-threatening - hepatitis, encephalitis, pneumonitis; mortality up to 50% if untreated
• Congenital herpes (transplacental - rare): Intrauterine HSV infection; presents at birth with skin vesicles/erosions, eye involvement, microcephaly; heals with characteristic reticulate scarring; usually fatal

• Less severe; local recurrences are managed conservatively
• Subclinical shedding still poses risk to neonate

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Neonatal Herpes [2 marks]

• Intrapartum (85%): Direct contact with infected maternal secretions during vaginal delivery - the most common route
• Postnatal (10%): From parent/caregiver with oral herpes (HSV-1)
• Transplacental/in utero (5%): Rare; transplacental hematogenous spread

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Management [1 mark]

Prevention

• Serology screening: Identify HSV-discordant couples; educate on avoidance of orogenital contact in 3rd trimester if partner is HSV-1 positive
• Suppressive antiviral therapy from 36 weeks: Acyclovir 400 mg TDS or valacyclovir 500 mg BD from 36 weeks to delivery in women with:
  • Initial episode of genital HSV during current pregnancy
  • History of recurrent genital herpes (to reduce clinical outbreaks and shedding at delivery)
  • Reduces need for cesarean section; reduces clinical recurrences by ~75%

Management of Active Infection During Pregnancy

• Primary/first-episode genital HSV in pregnancy: Treat with acyclovir 400 mg TDS for 10 days (all trimesters; avoid only in first month if possible due to theoretical spontaneous abortion risk)
• Recurrent episodes: Treat with acyclovir 400 mg TDS for 5 days

Mode of Delivery

• Cesarean section indicated when active genital lesions OR prodromal symptoms (tingling, burning) are present at onset of labor
• Reduces transmission from 8% to 1% in culture-positive mothers
• Does not prevent all neonatal herpes (20% of cases occur after cesarean)
• Cesarean should be offered if primary infection occurred in last 6 weeks of pregnancy (very high shedding)

Intrapartum Precautions

• Avoid fetal scalp electrodes (increase risk 7-fold)
• Avoid vacuum extraction (increases risk 2-27 fold)
• If membranes ruptured >6 hours with active HSV, discuss risks; cesarean still preferred but benefit diminishes

Neonatal Treatment

• All neonates with suspected/confirmed herpes: IV acyclovir 20 mg/kg every 8 hours for 14 days (SEM) or 21 days (CNS/disseminated)
• Post-suppressive oral acyclovir for 6 months after disseminated/CNS disease
• Andrews' Diseases of the Skin, pp. 857-867; Harrison's Principles of Internal Medicine 22E

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Q9b. Non-Treponemal Serological Tests for Syphilis [5 Marks]

Introduction (0.5 mark)

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Basis and Principle (1 mark)

• During syphilis, T. pallidum damages host cell membranes, releasing cellular phospholipids (primarily cardiolipin)
• These modified lipids act as haptens and stimulate production of reagin (non-specific IgG + IgM antibodies)
• Tests use cardiolipin-lecithin-cholesterol as the antigen
• Antigen-antibody interaction produces flocculation (visible precipitation/clumping) - read as positive
• Titration is possible (serial doubling dilutions: 1:1, 1:2, 1:4, 1:8... etc.); higher titer = more active disease

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Types of Non-Treponemal Tests [2 marks]

1. VDRL (Venereal Disease Research Laboratory) Test

• Flocculation test performed on a glass slide using cardiolipin-lecithin-cholesterol antigen
• Antigen-antibody reaction produces visible flocculation (clumping of antigen particles)
• Read microscopically (100-200x magnification)

• Sensitivity: 78-86% in primary, ~100% in secondary, ~71% in latent syphilis
• Specificity: ~98% (non-treponemal tests have more false positives than treponemal tests)
• Becomes reactive 1-3 weeks after chancre appears (4-6 weeks after infection)

• Standard test for screening and monitoring treatment response
• Gold standard for CSF testing in neurosyphilis - VDRL-CSF has high specificity; CSF-FTA-ABS used for sensitivity
• Quantitative titres fall 4-fold (2 dilutions) within 3-6 months of successful treatment; failure to do so suggests treatment failure, re-infection, or neurosyphilis

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2. RPR (Rapid Plasma Reagin) Test

• Macroscopic flocculation/agglutination test using carbon-particle antigen (cardiolipin coated onto charcoal particles)
• Read with the naked eye (visible black clumps vs. uniform suspension)
• Can be performed on unheated plasma (unlike VDRL which requires heat-inactivated serum)

• Does not require microscope - faster and more practical for field use/screening programs
• Can be automated (RPR-card test, also called Reagin Screen Test)
• Good correlation with VDRL in quantitative titres

• Sensitivity similar to VDRL; slightly less sensitive in early primary syphilis
• Cannot be used for CSF testing (only VDRL is validated for CSF)

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3. TRUST (Toluidine Red Unheated Serum Test) and USR (Unheated Serum Reagin)

• Modifications of VDRL; use toluidine red and charcoal as macroscopic markers
• Require no heating; economical alternatives for large-scale screening
• TRUST has sensitivity comparable to RPR

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Interpretation and Titres [1 mark]

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False Positives (Biological False Positives - BFP) [0.5 mark]

• Viral infections: EBV (infectious mononucleosis), hepatitis, HIV, chickenpox
• Bacterial: TB, leptospirosis, sub-acute bacterial endocarditis, typhoid
• Rickettsial disease
• Malaria
• Post-immunization

• SLE and other autoimmune diseases (antiphospholipid antibodies are a cause)
• Antiphospholipid syndrome (APS)
• Rheumatoid arthritis
• Elderly patients (aging)
• Leprosy (particularly LL)
• Intravenous drug abuse
• Pregnancy

• Robbins & Kumar Basic Pathology; Harrison's Principles of Internal Medicine 22E

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Q10a. Diagnosis of Chlamydia trachomatis in Men [5 Marks]

Introduction (0.5 mark)

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Clinical Presentation in Men (0.5 mark)

• Urethritis: Dysuria, urethral discharge (mucopurulent or watery) - often mild; may be absent
• Epididymo-orchitis: Unilateral scrotal pain and swelling in young sexually active men
• Reactive arthritis (Reiter syndrome): Urethritis + arthritis + conjunctivitis triad; occurs weeks after infection
• Proctitis: In men who have sex with men (MSM); tenesmus, rectal discharge
• Pharyngitis: From orogenital contact
• Asymptomatic: In up to 50% of cases

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Diagnostic Methods [3.5 marks]

A. Nucleic Acid Amplification Tests (NAATs) - Gold Standard

• Principle: Amplify C. trachomatis nucleic acids (plasmid DNA, chromosome DNA, rRNA) using PCR, TMA (transcription-mediated amplification), or SDA (strand displacement amplification)
• Specimen type for men:
  • First-catch urine (FCU): Patient must not have voided for 2 hours prior; collect the first 10-15 mL of urinary stream (contains highest concentration of urethral cells)
  • Urethral swab: Insert 2-3 cm into urethra; Dacron or rayon swab (not cotton - inhibits PCR)
  • Rectal swab for MSM with proctitis
  • Pharyngeal swab for oropharyngeal exposure
• Performance:
  • Sensitivity: 93-96% (superior to all other methods)
  • Specificity: >99%
  • Can simultaneously test for N. gonorrhoeae (dual NAAT)
• Available platforms: Abbott RealTime CT/NG, Roche Cobas 4800, Hologic Aptima Combo 2, BD Viper
• Advantages: No live organisms needed; detects asymptomatic infection; non-invasive (urine); rapid turnaround (2-4 hours to same day)
• Disadvantage: Expensive; cannot assess antibiotic susceptibility

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B. Cell Culture

• Gold standard historically but now largely replaced by NAAT in clinical practice
• C. trachomatis is grown in McCoy or HeLa-229 cell lines treated with DEAE-dextran or centrifugation inoculation
• Specimens: Urethral swab, first-catch urine
• Detection: Intracytoplasmic inclusion bodies visualized by:
  • Fluorescein-conjugated monoclonal antibody staining (Syva MicroTrak)
  • Iodine staining (glycogen-containing inclusions stain brown)
• Sensitivity: 70-85% (lower than NAAT due to fastidious nature, transport requirements)
• Advantages: Confirms viable organism; allows antimicrobial susceptibility testing; medicolegal gold standard (e.g., rape cases)
• Disadvantage: Requires specialized lab; 48-72 hour delay; expensive; transport conditions critical (cold chain)

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C. Direct Fluorescent Antibody (DFA) Test

• Principle: Fluorescein-labelled monoclonal antibodies staining C. trachomatis elementary bodies (EBs) directly on a smear
• Specimen: Urethral swab smear on glass slide
• Read under fluorescence microscope: EBs appear as bright apple-green dots (0.2-0.3 μm)
• Sensitivity: ~80-85%; Specificity: ~99%
• Rapid (1-2 hours), low cost
• Subjective (requires experienced microscopist)
• Useful in resource-limited settings

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D. Enzyme Immunoassay (EIA) and Enzyme-Linked Immunosorbent Assay (ELISA)

• Detect C. trachomatis lipopolysaccharide (LPS) antigen (genus-specific) in specimens
• Sensitivity: ~67-75% (substantially lower than NAAT)
• Specificity: ~97-99%
• Now largely obsolete in resource-adequate settings; still used where NAATs unavailable

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E. Gram Stain and Microscopy (for urethritis assessment)

• Not diagnostic for C. trachomatis specifically (organism too small to see on light microscopy)
• Gram-stained urethral smear establishes the presence of urethritis: ≥2 neutrophils per 1000x field
• Absence of gram-negative intracellular diplococci + urethritis = non-gonococcal urethritis (NGU) → warrants empiric treatment and NAAT for C. trachomatis
• This smear also rules in/out gonorrhea (gram-negative diplococci = 98% sensitive for gonococcal urethritis)

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F. Serology

• IgG, IgA antibodies against C. trachomatis by microimmunofluorescence (MIF) or ELISA
• Limited utility for acute genital infection in men: high background seropositivity; cannot distinguish active from past infection
• More useful for: lymphogranuloma venereum (LGV; serovars L1-L3), pelvic inflammatory disease workup, infertility evaluation
• MIF titres ≥1:256 suggest active systemic or LGV infection

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Treatment [0.5 mark]

• First-line: Doxycycline 100 mg BD for 7 days (preferred; superior eradication rates)
• Alternative: Azithromycin 1 g single oral dose (convenient but higher recurrence with M. genitalium co-infection)
• For LGV (L1-L3): Doxycycline 100 mg BD for 21 days
• Test-of-cure not routinely recommended unless symptoms persist or re-exposure likely
• Partner notification and treatment mandatory
• Harrison's Principles of Internal Medicine 22E, pp. 877-893

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Q10b. Classification of Balanoposthitis [5 Marks]

Introduction (0.5 mark)

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Classification [4 marks]

A. Infective Balanoposthitis

• Caused by Candida albicans (>90%)
• Risk factors: diabetes mellitus (most important), recent antibiotic use, obesity, sexual transmission from partner with vaginal candidiasis
• Clinical: Erythematous, moist, glazed glans with satellite papules/pustules, white curdy discharge, intense pruritus
• Diagnosis: KOH preparation showing pseudohyphae and budding yeasts; swab culture
• Treatment: Topical clotrimazole, miconazole, or nystatin; oral fluconazole 150 mg single dose for recurrent/severe cases; manage underlying diabetes

• Polymicrobial; anaerobes (Bacteroides, Fusobacterium), coliforms, streptococci
• Gardnerella vaginalis (associated with female partner's bacterial vaginosis) is increasingly recognized
• Clinical: Malodorous purulent/watery discharge, erythema, superficial erosions; prepuce becomes scarred with recurrent episodes
• Circinate balanitis (Reiter syndrome): Superficial erosions and shallow ulcers with a circinate (ring-like) edge on the glans; associated with chlamydial urethritis and reactive arthritis (Reiter syndrome = urethritis + arthritis + conjunctivitis + circinate balanitis)
• Treatment: Metronidazole 400 mg BD + amoxicillin-clavulanate

• Gonococcal: Urethritis with spread to glans; purulent discharge
• Chlamydial: Circinate erosions (Reiter)
• Trichomonas vaginalis: Transient erythema, pruritus
• Herpes simplex: Grouped vesicles, erosions, ulcers on glans; painful; recurrent
• Primary syphilis: Painless indurated ulcer (chancre) on glans or prepuce
• HPV: Condylomata on glans

• Tuberculosis of the genitalia
• Leprosy (glans involvement very rare)

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B. Dermatological/Inflammatory Balanoposthitis

• Chronic, benign, idiopathic; most common in uncircumcised middle-aged to elderly men
• Etiology: Poor hygiene, friction, moisture beneath prepuce
• Clinical: Well-demarcated, shiny, moist, erythematous, orange-red patch on glans/inner prepuce; studded with minute "cayenne pepper" spots (hemosiderin deposits from dilated capillaries)
• Histology: Dense dermal plasma cell infiltrate, dilated capillaries, hemosiderin; epidermal spongiosis; interface changes
• Treatment: Improved hygiene; topical steroids; tacrolimus; circumcision is curative; CO₂ laser

• Chronic progressive sclerotic disease affecting glans and prepuce
• Clinical: White, atrophic, sclerotic plaques on glans; phimosis (scarring of prepuce); meatal stenosis; urethral stricture in advanced cases; loss of preputial frenulum
• Association with squamous cell carcinoma (SCC) of penis (~5%)
• Histology: Homogeneous hyalinization of upper dermis; band of lymphocytes below; epidermal atrophy with loss of rete ridges; hyperkeratosis
• Treatment: Ultra-potent topical corticosteroids (clobetasol 0.05%); tacrolimus; circumcision; meatoplasty for stenosis

• Part of genital psoriasis; may be isolated or with body psoriasis
• Clinical: Well-demarcated, non-scaly (moist environment), red plaques on glans; inverse psoriasis pattern
• Koebner phenomenon; may be only manifestation of psoriasis in some
• Treatment: Mild topical corticosteroids; calcineurin inhibitors (tacrolimus, pimecrolimus); avoid potent fluorinated steroids on mucosa

• Annular, violaceous, flat-topped papules and plaques on glans
• Wickham's striae may be visible; erosive LP causes painful erosions
• Treatment: Topical corticosteroids; retinoids; circumcision may help

• Glans is the most common site for FDE in men
• Round, dusky-red to pigmented lesion at the same site with each re-exposure
• Common causative drugs: cotrimoxazole (most common), NSAIDs, tetracyclines, metronidazole
• Diagnosis: Oral provocation challenge (small dose); patch test on residual pigmented area

• Irritant or allergic; from condom latex, spermicides, lubricants, topical antiseptics (potassium permanganate, povidone iodine), partner's vaginal products

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C. Premalignant and Malignant Conditions (0.5 mark)

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D. Miscellaneous (0.5 mark)

• Diabetic balanoposthitis: Recurrent candidal or bacterial; glycosuria provides culture medium; early manifestation of undiagnosed diabetes
• Reactive (circinate) balanitis: Reiter syndrome (now preferred term: reactive arthritis)
• Traumatic: Friction, over-vigorous washing, zip injury
• Non-specific balanoposthitis: Commonest type; poor hygiene + phimosis + moisture; smegma accumulation

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Summary Table (0.5 mark)

• Andrews' Diseases of the Skin; Bailey & Love's Surgery; Harrison's Principles of Internal Medicine 22E

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Format note for examiners: Q6 is a full 10-mark answer (long essay). Q7a, 7b, 8a, 8b, 9a, 9b, 10a, 10b are each structured as 5-mark short notes with introduction (0.5), body (4 marks across subheadings), and a brief summary/table (0.5). All answers are suitable for 3rd-year Dermatology PG theory examination standard.